Corporate Overview January 2022 Nasdaq: ANAB

2 This presentation and any accompanying oral presentation contains forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995, including, but not limited to: the timing of initiation of the Company’s clinical trials, including rosnilimab’s clinical trials in rheumatoid arthritis and in a second indication and ANB032’s clinical trial in atopic dermatitis; the timing of the release of data from the Company’s clinical trials, including imsidolimab’s Phase 3 clinical trial in GPP, rosnilimab’s Phase 2b clinical trial in rheumatoid arthritis and ANB032’s Phase 2b clinical trial in atopic dermatitis; the timing of ANB033’s IND filing; statements regarding efficacy, safety and proof of mechanism from blinded data from rosnilimab’s clinical trial in alopecia areata; the Company’s ability to find a licensing partner for imsidolimab or etokimab and the timing of any such transaction; and the Company’s projected cash runway. Statements including words such as “plan,” “continue,” “expect,” or “ongoing” and statements in the future tense are forward-looking statements. These forward-looking statements involve risks and uncertainties, as well as assumptions, which, if they do not fully materialize or prove incorrect, could cause its results to differ materially from those expressed or implied by such forward-looking statements. Forward-looking statements are subject to risks and uncertainties that may cause the company’s actual activities or results to differ significantly from those expressed in any forward- looking statement, including risks and uncertainties related to the company’s ability to advance its product candidates, obtain regulatory approval of and ultimately commercialize its product candidates, the timing and results of preclinical and clinical trials, the company’s ability to fund development activities and achieve development goals, the company’s ability to protect intellectual property and other risks and uncertainties described under the heading “Risk Factors” in documents the company files from time to time with the Securities and Exchange Commission. These forward-looking statements speak only as of the date of this presentation, and the company undertakes no obligation to revise or update any forward-looking statements to reflect events or circumstances after the date hereof. Certain information contained in this presentation may be derived from information provided by industry sources. The Company believes such information is accurate and that the sources from which it has been obtained are reliable. However, the Company cannot guarantee the accuracy of, and has not independently verified, such information. The trademarks included herein are the property of the owners thereof and are used for reference purposes only. Such use should not be construed as an endorsement of such products. Safe Harbor Statement

3 Best-In-Class Immune Cell Modulating Antibodies Potential to restore immune balance across autoimmune and inflammatory diseases Strong capital position ~4 years of cash with >$575mm as of YE 2022 GSK immuno-oncology financial collaboration Significant royalty potential Research-driven Preclinical pipeline of immunology targets Immune Cell Modulators ANB033 (CD122 antagonist) IND-enabling Imsidolimab (IL-36r) P3 in GPP Etokimab (IL-33) P2b/3-ready in respiratory disorders Cytokine Antagonists (legacy programs for outlicensing) Rosnilimab (PD-1 agonist) P2b in Rheumatoid Arthritis ANB032 (BTLA agonist) P2b in Atopic Dermatitis Autoimmune and inflammatory diseases including dermatology, gastroenterology and rheumatology

4 Immune Cell Modulator Development Plan Three phase 2 initiations in 2023 Antibody Program Therapeutic Indication Development Stage and Anticipated Milestones Lead Optimization IND Enabling Phase 1 Phase 2 Phase 3 Rosnilimab (PD-1 agonist) Rheumatoid Arthritis Inflammatory Disease ANB032 (BTLA agonist) Atopic Dermatitis ANB033 (CD122 antagonist) Inflammatory Diseases Imsidolimab (IL-36r antagonist) Generalized Pustular Psoriasis (GPP) Etokimab (IL-33 antagonist) Respiratory Disorders P2b initiation Q3 2023 Top-line data mid 2025 Trial initiation YE 2023 P2b initiation Q2 2023 Top-line data YE 2024 IND submission H1 2024 Top-line data Q4 2023 P2b/3-ready All programs discovered internally using AnaptysBio’s proprietary antibody platform technology Legacy Programs Available for Outlicensing Im m u n e C e ll M o d u la to rs C yt o ki n e A n ta go n is ts Outlicense prior to FDA Approval no further internal investment

Advantages of Immune Cell Modulation in Treatment of Autoimmune and Inflammatory Diseases

6 Moderate-to-Severe Inflammatory Diseases are Complex, Leading to Shortcomings in SOC Therapies Breadth of mechanism Cell signaling inhibitors: efficacy ceiling with AEs at most effective doses TYK2 (next gen) • Complex, heterogeneous diseases involve upregulation of multiple cytokines • Treatment requires more than a single cytokine blocker Efficacy • Downstream intervention does not target underlying dysregulation • Chronic treatment required to suppress symptoms Durability • Cell signaling inhibitors (e.g. JAKi) with broad activity, have significant tox - Black-box warning risks include major cardiac and thrombotic events Safety Single Cytokine blockers TYK2 (Sotyktu; suboptimal PD) E ff ic a c y On-target activity (acceptable tox) Off-target activity (unacceptable tox) JAKi (IC90) JAKi (Approved doses; suboptimal PD)

7 JAKi (IC90) JAKi (Approved doses; suboptimal PD) Immune cell modulators: Potential for increased breadth, depth and durable response E ff ic a c y Single Cytokine blockers TYK2 (Sotyktu; suboptimal PD) Breadth of mechanism On-target activity (acceptable tox) Off-target activity (unacceptable tox) TYK2 (next gen) • Suppression of immune cells may increase breadth and depth of response Efficacy: Act directly on dysregulation • Restore tolerance by modulating key immune cell types • Potential for durable response Durability: Longer remission • Preferential target expression on activated immune cells may enable wider therapeutic window • Growing agonist class experience has been well-tolerated to date • No evidence of carcinogenicity with checkpoint inhibitors in I&I, such as abatacept, in decades of use Safety: Targeting immune cells Immune Cell Modulators May Restore Immune Balance Across Moderate-to-Severe Complex Diseases

8 ANB033 (CD122 antagonist) ANB032 (BTLA agonist) Rosnilimab (PD-1 agonist) A d ap ti ve Im m u n it y B cells Trm Tcon Treg/Tcon ratio In n at e im m u n it y NK cells ILCs Dendritic cells Potential Mechanisms of Action 1 Bias Treg/Tcon ratio towards tolerance at sites of aberrant inflammation and systemically Potential to deplete (rosnilimab) or induce death (ANB033) in pathogenically targeted activated cells 4 Effector function (Fc region) Depletion potential (IgG1) Non-depleting (IgG4) Non-depleting (undisclosed) Modulation of innate immunity may support return to homeostasis 3 2 Modulation of adaptive immunity may enable resolution of inflammatory cycle (Activated PD-1+ T cells) Immune Cell Modulators Immune Cell Modulators are a Novel Therapeutic Class Suppress activated immune cell types to restore immune balance

9 • Checkpoint agonists for PD-1 and BTLA down regulate T cell mediated immune responses - BTLA also present on B cells and dendritic cells • Potential applicability across complex diseases - Dermatology - Gastroenterology - Rheumatology - Respiratory - Neurology • Potential for concomitant or sequential combination with targeted immune- suppressive therapies Immune Cells (e.g., T, B, dendritic) Checkpoint receptors (e.g. PD-1, BTLA) Treat cancer (can lead to inflammatory disorders) Checkpoint antagonists potentiate immune cells Checkpoint agonists downregulate immune cells Treat inflammatory disorders Anti-Inflammatory Checkpoint Agonist Antibodies

10 Phosphatase Kinase Tighter synapse* Looser synapse* • Antigen binding epitope: - Spare natural ligand binding interaction - Bind proximal to the membrane to enhance tight synapse formation • Antigen binding affinity: - Optimal (not maximal affinity) Antigen binding characteristics • Fc receptor binding affinity: - Tight synapse formation - Clustering of checkpoint receptors promoted via Fc anchoring • Effector function: - Isotype selection may enable depletion (NK cell-mediated ADCC and/or monocyte-mediated ADCP) Fc binding characteristics Tight immune synapse optimizes agonistic activity by excluding large phosphatases that dephosphorylate the checkpoint receptor *Figure adapted from Frontiers in Immunology. 2018 Oct 8; 9: 2306 Combination of Characteristics Optimize Agonistic Signaling

Rosnilimab (PD-1 agonist mAb) Introduction

Rosnilimab Fc Receptor PD-1 PD-L1 P SHP2 Antigen Presenting Cell T Cell Rosnilimab: Best-in-Class PD-1 Agonist Antibody Suppression of T cell mediated inflammatory diseases • Rosnilimab: IgG1 antibody that binds to PD- 1+ T cells - Membrane proximal binding epitope contributes to differentiated potency • Acts on inflamed tissue and periphery to: - Mimic PD-L1 function to down-regulate T cell activity (agonistic signaling) - Deplete PD-1+ T cells (effector function) - Prevent migration of PD-1+ T cells to inflamed tissue by peripheral depletion • Specific expression on activated T cell subclasses (e.g. Th1, Th2, Th17) • Rosnilimab targets multiple distinct inflammatory mechanisms addressed by approved therapies (CD80/86 modulator) (S1PR inhibitor) (α4β7 blockers) Inhibit T cell proliferation and cytokine secretion Deplete PD-1+ T cells Prevent migration of pathogenic T cells to inflamed tissue Rosnilimab MOA -- 12

• Rosnilimab shows meaningful IFNγ inhibition beginning at low concentrations • Potency differentiation from Lilly’s PD-1 agonist is sustained across clinical concentrations Tetanus toxoid recall stimulation assay measures antigen- specific immune cell response. Prior immunity in majority of population due to tetanus vaccination, N=9 0.01 0.1 1 10 100 -100 -50 0 50 100 5 Day PBMC TT recall assay n = 9 healthy donors Antibody (nM) % i n h ib it io n I F N -γ (n o rm a li z e d t o i s o ty p e ) Rosnilimab LLY PD-1 agonist Rosnilimab Lilly PD-1 agonist Rosnilimab LLY -100 -50 0 50 1.24 nM Antibody % i n h ib it io n I F N -γ ✱✱✱✱ Rosnilimab LLY -100 -50 0 50 3.7 nM Antibody % i n h ib it io n I F N -γ ✱✱✱✱ Rosnilimab LLY -100 -50 0 50 11.1 nM Antibody % i n h ib it io n I F N -γ ✱✱✱✱ Lilly PD-1 agonist Lilly PD-1 agonist Lilly PD-1 agonist Rosnilimab Significantly Reduces IFNγ in Healthy PBMCs Compared to Lilly PD-1 Agonist 13

Rosnilimab Demonstrates Superior Agonistic Signaling and Depletion of PD-1+ T Cells at Clinically Relevant Concentrations 0.1 1 10 100 0 20 40 60 80 100 120 Antibody (nM) % P ro li fe ra ti n g T c e ll s (n o rm a li z e d t o i s o ty p e ) Lilly PD-1 agonist Rosnilimab 0 0.001 0.01 0.1 1 10 100 0 20 40 60 80 100 120 Antibody (nM) P e rc e n t o f U n tr e a te d Isotype Control Rosnilimab Lilly PD-1 Agonist Anti-CD3+ anti-CD28 stimulation of PBMCs for proliferation assessment of T cells, representative data from N=4 donors Agonistic Signaling (Inhibition of T cell proliferation) Depletion (NK cell-mediated ADCC of PD-1+ T cells) Healthy donor T cells + NK cells (1:5 ratio) + rosnilimab in in- vitro ADCC assay, representative data from N=2 donors Complementary mechanisms of action enable potent reduction of PD-1+ T cells to restore immune balance 14

Rosnilimab Healthy Volunteer Phase 1 Trial Results Potent and sustained reduction in peripheral PD-1+ T cells for >30 days in SAD -100 -80 -60 -40 -20 0 20 1 5 8 15 22 29 43 85 P e rc e n t C h a n g e F ro m B a s e li n e M e a n ( S E ) Days Treg Tcon PD-1+ Tcon PD-1 high Tcon ✓ Well tolerated with no dose-limiting toxicities ✓ Favorable PK with ~2 week half-life with IV or SC dosing ✓ Full RO observed quickly and maintained for 30 days with a single dose Favorable safety, pharmacokinetics and pharmacodynamic activity • PD-1+ T cell effect - >50% reduction of PD-1+ Tcon - >90% reduction of PD-1 high Tcon • PD-1 negative Tcon effect - Minimal/no effect • Treg effect - Minimal /no effect on overall Tregs - Positive bias to Treg/Tcon ratio *Results shown from 400mg subcutaneous dose (SAD) 15

Rosnilimab 400 mg SC q4w N = 4 5 R an d o m iz ed 2 :1 Placebo Treatment Period Follow-Up Period W e e k 0 W e e k 2 4 W e e k 3 2 W e e k 2 0 Last Dose “Proof of Mechanism” P2a Blinded Pooled Interim Data Peripheral T cell effect • Impact on activated T cells and Tcon / Treg ratio in blood and implications for broader inflammatory diseases through week 32 ✓ Robust reductions in peripheral PD-1+ T cells observed in AA patients consistent with HV P1 trial Change in SALT score (primary endpoint) • Commercially relevant in absolute SALT <20 (secondary endpoint) X Modest improvement in some patients observed through week 24+; No patients with absolute SALT<20 Durability • Maintenance of change in SALT score through week 32 • TBD; patients with SALT improvement observed were stable off treatment through weeks 28 - 32 Safety and tolerability ✓ Generally safe and well tolerated Additional P2a Data Available H2 23 • Tissue Biopsies - Impact on reduction of PD-1+ T cells and cytokines in hair follicle (inflamed tissue) • Circulating Biomarkers & T Cell Phenotyping - Impact on reduction of PD-1+ T cells, including Tregs and Tcons, and cytokines in periphery Rosnilimab “Proof of Mechanism” Phase 2a Trial in Moderate-to-Severe Alopecia Areata 16

-100 -80 -60 -40 -20 0 20 1 2… 8… 1… 1… 2… P e rc e n t C h a n g e F ro m B a s e li n e M e a n ( S E ) Treg Tcon PD-1+ Tcon PD-1 high Tcon 0 (n=51) Week 4 (n=42) Week 12 (n=33) Week 24 (n=22) Week 28 (n=16) Week 32 (n=14) Blinded (pooled treated + placebo 2:1 randomization) Immunophenotyping Data Last dose Week 20 • PD-1+ T cell effect - >60% reduction of PD-1+ Tcon - >80% reduction of PD-1 high Tcon • PD-1 negative Tcon effect - Minimal/no effect • Treg effect - Minimal /no effect on overall Treg - Positive bias to Treg/Tcon ratio PD-1+ T cell impact in the periphery supports proof of mechanism to advance rosnilimab into additional indications, such as rheumatoid arthritis *Results shown at 400mg subcutaneous dose Q4W Rosnilimab P2a “Proof-of-Mechanism” Blinded Data Potent and sustained reduction in peripheral PD-1+ T cells in alopecia patients consistent with HV P1 trial results 17

Rosnilimab (PD-1 agonist mAb) Rheumatoid Arthritis (RA)

19 Initiation of Autoimmunity Pre-symptomatic RA Mild RA Moderate-to-Severe RA CD3+ T cells PD-L1PD-1+ *Adapted from Nature Reviews Disease Primers volume 4, Article number: 18001 (2018) and PLoS One 2018; 13(2): e0192704 PD-1+ T Cells are Clinically Validated Drivers of Disease in RA >80% of T cells in treatment-naive RA joints are PD-1+ and not down-regulated due to lack of sufficient PD-L1 expression

20 PD-1 PD-1 Rosnilimab *Adapted from Nature Reviews Disease Primers volume 4, Article number: 18001 (2018), **b/tsDMARD – biologic/targeted synthetic disease modifying antirheumatic drug, LDA – low disease activity PD-1 Agonists are a Promising Novel Mechanism for the Treatment of RA • b/tsDMARDs provide benefit by inhibiting either T cells, B cells or downstream cytokines • However, most patients cycle through classes of therapy - Many patients cannot achieve LDA - If LDA achieved, responses often not durable • PD-1 agonists target multiple distinct inflammatory mechanisms addressed by approved therapies to treat RA - Inhibit PD-1+ T cell proliferation and cytokine secretion - Deplete PD-1+ T cells, including impact on downstream B cells - Prevent migration of pathogenic PD-1+ T cells to joints

21 • Target population in US generated ~$10 billion in 2021 - Rituxan (typically salvage therapy) achieves well over $1 billion sales in 3L+ RA despite infection risk • No new therapeutic class has launched for RA since JAK inhibitors (Xeljanz) a decade ago (2012) • Lack of established SOC in 2L+ provides opportunity for new class to penetrate - Comparable or differentiated efficacy - Durable responses - Treatment of salvage population Rheumatoid Arthritis US Prevalence ~1.8 Million Treated ~1 Million Treated with biologics and JAKs (b/tsDMARDs) ~500,000 2L (e.g. TNF-experienced) >100,000 Salvage (do not achieve LDA on any treatment) ~55% ~45% ~25% Target Population RA is a Substantial Opportunity for a New Class of Biologics ~500k patients in the US seek treatment after progressing on anti-TNF therapy *Claims analysis to determine market size based on 5 years of claims history, ** Evaluate Pharma,***b/tsDMARD – biologic/targeted synthetic disease modifying antirheumatic drug, 2L – 2nd line

22 -40 -30 -20 -10 0 0 2 4 8 12 14 16 20 24 C h a n g e F ro m B a s e li n e Weeks CDAI* Lilly’s PD-1 Agonist Showed Proof of Mechanism and Promising Efficacy in a Phase 2a RA Study • 48% and 61% of patients achieved LDA at week 12 for 300 and 700 mg Q4Q IV doses • Patients achieving LDA at week 12 continued treatment through week 24 - At either dose, patient benefit was sustained • Similar responses observed regardless of whether a patient was naïve to or had received a prior b/tsDMARD Period 1 Period 2 * *** * *** Placebo (N=24) Peresolimab 300mg (N=25) Peresolimab 700mg (N=49) Peresolimab 300mg (N=12) Peresolimab 700mg (N=30) Patients achieving CDAI** LDA at Week 14 continued on peresolimab *Week 0 though Week 24 data estimated from peresolimab (PD-1 agonist) 2022 ACR presentation,**CDAI – clinical disease activity index, LDA – low disease activity

23 63% 71% 62% 60% 65% 51% 71% 74% 29% 45% 32% 32% 36% 26% 42% 57% 13% 25% 10% 17% 18% 10% 20% 35% 0% 25% 50% 75% 100% Adalimumab (TNF) Upadacitinib (JAK) Adalimumab (TNF) Abatacept (CD80/86) Sarilumab*** (IL-6) Rituximab**** (CD20) Peresolimab (700mg Week 12) Peresolimab (700mg Week 14) % R e s p o n d e r ACR20 ACR50 ACR70 Lilly PD-1 agonist: 2a data reported at ACR 2022 SELECT-COMPARE Study AMPLE Study** Population in 700mg arm: 63% patients MTX-IR, 37% patients b/tsDMARD-IR ACR Scores at Week 12 in MTX-IR Patients* Fragmented market No clear treatment of choice after failure of anti-TNFs PD-1 Agonists have the Potential to Restore Immune Balance and Differentiate from Available Treatments on ACR50/70 *Patients on background MTX, **12 week data based on ACR time graph, unless otherwise noted. ***Phase 3 study versus placebo in MTX-IR patients, **** Phase 3 study versus placebo in MTX- IR patients (SERENE) at week 24, *****5 year claim history analysis CD20, 19%IL-6, 19%JAK, 27%CD80/86, 35% US Market Share of 2L (TNF-experienced) RA Therapies*****

24 Inhibition of T Cell Proliferation (in RA Patient-Derived PBMCs) • More potent reduction compared to Lilly PD-1 agonist is consistent between healthy PBMCs and RA patient- derived PBMCs Anti-CD3+ anti-CD28 stimulation of PBMCs for proliferation assessment of T cells, representative data from N=3 donors 0 0.1 1 10 100 0 20 40 60 80 100 Antibody (nM) % P ro li fe ra ti n g T c e ll s (n o rm a li z e d t o i s o ty p e ) Isotype Control Lilly PD-1 Agonist Rosnilimab 0 Rosnilimab Demonstrates Superior Inhibition of T Cell Proliferation in Rheumatoid Arthritis Patient-Derived PBMCs

25 • Explore broad exposure response and establish efficacious dose • Enable initiation of a registrational phase 3 campaign • Analyze potential predictive baseline characteristics including patient prior therapy and biomarkers • Three dose levels of rosnilimab - High dose is multiple fold higher than used in alopecia areata Phase 2a study • Subcutaneous dosing to support patient self-administration • Rosnilimab dosing duration of ~6 months • Global, multi-hundred patient placebo- controlled trial • Inclusive broad population of cDMARD and b/tsDMARD-experienced patients • Standard efficacy endpoints including ACR20/50/70, DAS28 and CDAI • Phase 2b trial initiation in Q3 2023 • Topline data anticipated in mid 2025 P2b Trial Objectives Patient Population and Endpoints Dosing and Administration Timing and Trial Initiation Rosnilimab P2b Trial in Moderate-to-Severe Rheumatoid Arthritis Initiation Q3 2023; Topline Interim Data Mid 2025 *cDMARD – conventional disease modifying antirheumatic drug, CDAI – clinical disease activity index, DAS28 – disease activity score

ANB032 (BTLA agonist mAb) Introduction

27 • ANB032: IgG4 antibody that binds to BTLA in lymphoid (T and B) cells and dendritic cells - Fc receptor binding profile together with membrane proximal binding epitope contributes to differentiated potency • ANB032 inhibits T cell proliferation and inflammatory cytokine secretion • ANB032 demonstrated robust in vivo efficacy in animal models of GVHD • Potential broad applicability to inflammatory disease due to breadth of BTLA expression across immune cell types ANB032: Best-in-Class BTLA Agonist Antibody Suppression of T and B cell mediated inflammatory diseases Pro-inflammatory immune cell activation by HVEM ligands x BTLA ANB032 + BTLA agonistic signal inhibits immune cell activity Th2 cell Th17 cell B cell Dendritic cell TregTh1 cell

28 ANB032 Demonstrates Superior Agonistic Signaling in Healthy PBMCs Compared to Lilly BTLA Agonist 0.1 1 10 100 40 60 80 100 120 140 Antibody (nM) % P ro li fe ra ti n g T c e ll s (n o rm a li z e d t o i s o ty p e ) 0 0.1 1 10 100 40 60 80 100 120 140 Antibody (nM) % I F N -γ S e c re ti o n (n o rm a li z e d t o i s o ty p e ) Isotype Control Lilly BTLA Agonist ANB032 0 Inhibition of T cell Proliferation Inhibition of Th1 Cytokine Secretion 0.1 1 10 100 40 60 80 100 120 140 Antibody (nM) % I L -1 7 A S e c re ti o n (n o rm a li z e d t o i s o ty p e ) 0 0.1 1 10 100 40 60 80 100 120 140 Antibody (nM) % I L -1 3 S e c re ti o n (n o rm a li z e d t o i s o ty p e ) 0 Inhibition of Th17 Cytokine Secretion Inhibition of Th2 Cytokine Secretion Anti-CD3+ anti-CD28 stimulation of PBMCs for proliferation assessment of T cells and cytokine secretion; representative data from N=4 donors ANB032 shows meaningful T cell inhibition beginning at low concentrations and potency differentiation is sustained across clinical concentrations

29 • 96 healthy volunteers in randomized, double- blind, placebo-controlled SAD and MAD cohorts • ANB032 well-tolerated with no dose limiting tox - Most AEs mild-to-moderate, of short duration, dose independent and resolved without sequelae - No Serious Adverse Events • Favorable PK: ~2-week half-life with IV and SQ dosing • Full receptor occupancy (RO) within hours and maintained for >30 days • Pharmacodynamic analyses: - Rapid and sustained target engagement on both T cells and B cells - Reduction of cell surface BTLA expression - Duration of reduced BTLA expression persisted in a dose-dependent manner ANB032 Phase 1 Healthy Volunteer Trial Top-Line Data Favorable safety, pharmacokinetics and pharmacodynamic activity T C e ll s B C e ll s Lower (Single) Dose Higher (Single) Dose 0 20 40 60 80 100 120 0 14 28 42 56 70 84 Study Day 0 20 40 60 80 100 120 0 14 28 42 56 70 84 Study Day 0 20 40 60 80 100 120 0 14 28 42 56 70 84 Study Day 0 20 40 60 80 100 120 0 14 28 42 56 70 84 Study Day 0 20 40 60 80 100 120 0 14 28 42 56 70 84 Study Day Higher Dose %RO Serum sBTLA (ng/mL) Total Cell Surface BTLA (% of Baseline) 0 20 40 60 80 100 120 0 1 28 42 56 70 84 Study Day Higher Dose %RO Serum sBTLA (ng/mL) Total Cell Surface BTLA (% of Baseline) ANB032 in humans mirrored observation in animal models of inflammation supporting potential broad treatment of T and B-cell driven inflammatory diseases

ANB032 (BTLA agonist mAb) Atopic Dermatitis Phase 2b

31 Th1Th2 ILC2 Th2 TRM TRM TRM TRM T T B Th17 Th2 Barrier dysfunction, innate immune activation and Th2-driven inflammation Antigen presentation, Th1 and Th17-driven inflammation Potential for BTLA expression Atopic Dermatitis (AD) is Broader than a Th2 Inflammatory Disease Th2 targeting SOC provides benefit; however, other cell types including Th1, Th17 and dendritic cells may contribute significantly to AD pathogenesis Adapted from Nature Reviews Disease Primers volume 4, Article number: 1 (2018) dupilumab amlitelimab Th22

32 • Dupixent is standard of care in moderate- to-severe AD - >$7 billion projected global sales (2027)** • Significant room to differentiate vs. SOC - Dupixent EASI75 of ~45%-50% leaves substantial opportunity for broader response, including suboptimal responding patients - Dupixent EASI90 of ~35% leaves substantial opportunity for deeper response - Potential for durable response - Black box warning is an impediment to use of oral JAKs Atopic Dermatitis US Prevalence* 5 Million Diagnosed 2 Million Diagnosed Moderate-to-Severe ~40% ~60% 1.2 Million Biologic eligible Moderate-to-Severe *Claims analysis to determine market size based on 5 years of claims history, ** Evaluate Pharma. Target Population AD is a Substantial Opportunity for a New Class of Biologics ~1.2m patients in the US are biologic eligible

33 0 20000 40000 60000 80000 IF N  [p g /m l] CD3/CD28 stimulation **** 0 20 40 60 80 IL -1 3 [ p g /m l] CD3/CD28 stimulation ** 0 250 500 750 1000 1250 1500 IL -1 7 A [ p g /m l] CD3/CD28 stimulation *** p<0.0001 **** p<0.001 *** p<0.01 ** (all at 100 nM) Inhibition of Th1 (IFNγ Cytokine Secretion) Inhibition of Th2 (IL-13 Cytokine Secretion) Inhibition of Th17 (IL-17A Cytokine Secretion) ANB032 Inhibits Th1/Th2/Th17 Cytokine Secretion in Atopic Dermatitis Patient-derived PBMCs

• Adult patients with moderate to severe atopic dermatitis • All comer population; includes patients with both Dupixent naïve and Dupixent experience Patient Population • Primary: Mean change from Baseline in EASI at Week 14 • Secondary: EASI75, IGA 0/1, PNRS, DLQI, SCORAD50, Safety • Exploratory: Th1/Th2/Th17 biomarkers, tissue biopsy Key Endpoints N = 1 6 0 R an d o m iz e 1 :1 :1 :1 Treatment Period W e e k 0 W e e k 1 4 Follow-Up Period W e e k 2 4 ANB032 Dose 1 Placebo ANB032 Dose 3 ANB032 Dose 2 Last dose Week 12 34 ANB032 P2b Trial in Moderate-to-Severe Atopic Dermatitis Initiation Q2 2023; Topline data YE 2024

ANB033 (anti-CD122 antagonist mAb) Autoimmune and Inflammatory Diseases

36 CD122 is a shared beta subunit of the receptors for IL-15 and IL-2 • IL-15 mediates survival of TRM cells • Both IL-15 and IL-2 mediate: - Proliferation of T cells - Inflammatory cytokine secretion (IFNγ) during T cell activation • High affinity antagonist antibody induces death in TRM cells by preferentially inhibiting the lower affinity dimeric receptor complex - Spares Tregs which express higher affinity IL-2 trimeric receptor complex • Targeted elimination of TRM cells may potentially drive durable responses ANB033 MoA: Induce death of TRM cells to achieve and maintain remission Tregs TRM cells CD122 CD122 ANB033 ANB033: Anti-CD122 Antagonist mAb Targets Pathogenic Tissue Resident Memory T Cells (TRM) IND filing targeted H1 2024

37 0 10 20 30 40 50 60 -20 -10 0 10 20 Average Body Weights (carried) Study Day W e ig h t C h a n g e ( % o f S ta rt ) • GVHD (severe phenotype) model in human IL-15 transgenic mouse supports T cell and NK cell survival • ANB033 preclinical data suggests targeted elimination of pathogenic TRM drives more potent and durable response than belatacept - Belatacept (GVHD standard-of-care which only impedes T cell activation) shows minimal benefit over control End of dosing Note: ANB033 treated mice dosed twice per week through Day 28 GVHD model is biologically relevant to CD122 antagonist MoA with translation to inflammatory diseases driven by pathogenic TRM and Treg imbalance including rheumatology, dermatology, gastroenterology, and respiratory ANB033: Durable Survival in GVHD Model All mice treated at high-dose survived well beyond end of dosing

Legacy Programs for Outlicense Imsidolimab (IL-36r antagonist mAb) Etokimab (IL-33 antagonist mAb)

39 • GPP is a systemic, life-threatening inflammatory disease characterized by widespread pustules - Associated with unregulated IL-36 signaling - Patients have a high fever and elevated levels of serum CRP and inflammatory cytokines (e.g., IL-8) - Severe GPP patients can die from cardio-pulmonary failure, exhaustion, toxicity and infection • GPP ICD-10 diagnostic code analysis by IQVIA assessed US prevalence during 2017-2019 timeframe - ~37,000 unique patients diagnosed at least once - ~15,000 unique patients diagnosed two or more times • FDA has granted Orphan Drug Designation to imsidolimab for the treatment of GPP • Worldwide registry (RADIANCE) of GPP patients ongoing – Increase understanding of patient journey and support enrollment of Phase 3 trial Generalized Pustular Psoriasis (GPP) Systemic inflammatory disease where IL-36 pathway plays key role in pathology

Normal Individuals IL-36 cytokine signaling balanced by functional IL-36 receptor antagonist Disease Patients Uncontrolled signaling due to dysfunctional IL-36 receptor antagonist or elevated IL-36 cytokine levels Treated Patients Anti-IL-36 antagonist antibody has the potential to dampen disease by blocking the IL-36 receptor 40 Dampened Inflammatory Response Dermatological Inflammatory Diseases Balanced Inflammatory Response Imsidolimab: an Anti-IL-36r Antagonist Antibody Uncontrolled-IL-36 signaling, as well as a genetic IL-36 association, mediates GPP

41 • Imsidolimab 750mg IV loading dose + 100mg SC q4w maintenance dose • Rapid and sustained efficacy through week 16 – 6 of 8 (75%) patients achieved primary endpoint of improvement in the clinical global impression scale (CGI) – Early reduction of erythema with skin pustules by week 1; sustained relative to baseline at week 16 – GPP Physician Global Assessment (GPPGPA) demonstrated sustained efficacy through week 16 – 2 patients dropped out of the study before Day 29 and deemed non-responders • Imsidolimab generally well-tolerated – Most adverse events were mild to moderate and resolved without sequelae – Two subjects had serious adverse events and recovered without sequelae (sepsis due to S. aureus infection and SARS-CoV-2 injection) • Genotypic testing indicated homozygous wild-type IL-36RN, CARD14 and AP1S3 alleles for all tested patients – IL-36R inhibition may be efficacious in GPP irrespective of genetic mutations Endpoint Baseline Week 1 Relative to Baseline Week 4 Relative to Baseline Week 16 Relative to Baseline CGI improvement (primary endpoint) N/A 7 of 8 patients 6 of 8 patients 6 of 8 patients mJDA-SI 9 -29% -54% -58% Erythema with pustules (% body surface area) 24% -60% -94% -98% DLQI (MCID of -4) 16 -1 -6 -11 Baseline Week 4 Week 16 GALLOP: Imsidolimab GPP Phase 2 Trial Top-Line Data Presented at EADV Congress October 2021

42 Patient Population R an d o m iz at io n n =4 5 * W e e k 0 Key Endpoints • Male and female subjects 18 to 80 years of age • Clinically confirmed diagnosis of GPP as per ERASPEN definition • Baseline Generalized Pustular Psoriasis Physician Global Assessment (GPPPGA) score of at least moderate severity (3 and higher) • Active flare with pustules and erythema accounting for at least 5% of body surface area at baseline • Primary: GPPPGA score of clear (0) or almost clear (1) at GEMINI-1 Week 4 • Key Secondary: Pustulation Rating Scale (PRS) of 0 or 1 at GEMINI-1 Week 1 • Other: Time to flare recurrence, proportion of subjects in remission, DLQI, safety Placebo (n=15) Responders (achieved GEMINI-1 Week 4 primary endpoint): Randomized 1:1 to q4w 200mg SC imsidolimab or q4w SC placebo W e e k 1 5 6 GEMINI-1: 4-Week Primary Endpoint W e e k 4 Partial Responders (improvement by GEMINI-1 Week 4 without achieving primary endpoint) or Non-Responders (no improvement without need for rescue): q4w 200mg SC imsidolimab Placebo-dosed non-responders who are rescued (eligibility after GEMINI-1 Week 1)** 750mg IV imsidolimab followed by q4w 200mg SC GEMINI-2: 3-Year Long-Term Extension * 80% power calculated for GEMINI-1 using two-sized test alpha of 0.05 assuming ~40% effect size with 45 patient sample size **Starting at week 1 in GEMINI-1, placebo patients who have not improved or are worsening are eligible to be rescued with imsidolimab W e e k 0 Imsidolimab 300 mg IV (n=15) Imsidolimab 750mg IV (n=15) GEMINI-1 & 2: Imsidolimab GPP Phase 3 Trials GEMINI-1 top-line data anticipated Q4 2023 ClinicalTrials.gov: NCT05352893, NCT05366855

• Etokimab: IgG1 antibody that inhibits the activity of the active form of IL-33 • IL-33 is genetically associated with asthma – IL-33 loss-of-function mutations protect against asthma, while gain-of-function mutations increase asthma incidence – Translational studies have demonstrated IL-33’s role as a pro-inflammatory cytokine released upon allergen contact with epithelium • Broad commercial opportunity in respiratory and allergic conditions – ~1.1 million adults diagnosed in U.S. with severe asthma – ~550,000 million adults diagnosed in U.S. with Type 2 or Non-Type 2 COPD are inadequately controlled by standard of care • IL-33 pathway derisked in COPD (positive Phase 2 data via AZ and REGN/SA) Etokimab: Phase 2b/3-Ready Anti-IL-33 Antagonist Antibody IL-33 biology applicable to respiratory disorders 43 • IL-33 is active in its reduced form and is quickly oxidized into an inactive form as a mechanism to limit its local activity • The majority of IL-33 in the body is the inactive oxidized form Given etokimab’s MOA, it specifically inhibits only the IL-33 molecules that are driving activity and not “wasted” by binding to non-active oxidized IL-33 Etokimab is P2b/3 Ready (drug supply on hand, preclinical toxicology, P2 data, and competitor POC data across respiratory diseases)

GSK Immuno-Oncology Financial Collaboration JEMPERLITM (dostarlimab, anti-PD-1 Antagonist) Cobolimab (GSK4069889, anti-TIM-3 Antagonist) GSK4074386 (TSR-033, anti-LAG-3 Antagonist)

45 JEMPERLI (anti-PD-1 antagonist) GSK anticipates ~$1.2-2.4B peak annual sales for JEMPERLI in currently approved indications and anticipated 1L endometrial/ovarian approvals* • JEMPERLI 12-25% royalties on annual net sales ≥ $1B • JEMPERLI $75mm commercial milestone on annual net sales ≥ $1B In 2H21, ANAB received $250mm upfront in exchange for only the above receivables until Sagard is paid back one of the following capped returns: : • $312.5MM (125% of upfront) by end 2026 or • $337.5MM (135% of upfront) by end 2027 or • $412.5MM (165% of upfront) anytime after 2027 Sagard: JEMPERLI Capped Non-Recourse Monetization Cobolimab (anti-TIM-3 antagonist) GSK4074386 (anti-LAG-3 antagonist) • Both programs being developed in combination with JEMPERLI • 4-8% royalties on annual net sales on each program • $5mm clinical development, $90mm regulatory and $165mm commercial milestones on each program** * In June 2021, GSK estimated potential peak annual global JEMPERLI sales on a non-risk adjusted basis of £1-£2 billion ** $10mm clinical development milestones remaining for GSK4074386 Note: Sale of ZEJULA (niraparib) royalty interest in September 2022 to wholly-owned subsidiary of DRI Healthcare Trust for $35mm upfront + $10mm potential milestone upon FDA approval of ZEJULA for the treatment of endometrial cancer, for which the drug is currently in a fully-enrolled ongoing RUBY Phase 3 study of dostarlimab + niraparib, to the extent that such approval occurs on or before 12/31/25. Significant Potential Royalties from Immuno-Oncology Financial Collaboration Receivables Excluded from Sagard Monetization • JEMPERLI 8% royalties on annual net sales <$1B • JEMPERLI $15mm regulatory and $90MM commercial milestones on annual net sales <$1B

46 (Anti-PD-1 antagonist) Cobolimab (Anti-TIM-3 antagonist) GSK4074386 (Anti-LAG-3 antagonist) Dostarlimab: 1L Endometrial Cancer • Approved in US and EU for dMMR recurrent or advanced endometrial cancer after progressing a platinum-containing regimen • P3 RUBY trial met primary endpoint in 1L primary advanced or recurrent endometrial cancer (Dec. 2022) – Regulatory submissions planned 1H 2023 – Significant market opportunity for 30% of the 65,000 new endometrial diagnoses per year in the US* Dostarlimab and cobolimab: NSCLC • P3 COSTAR trial (combination of dostarlimab + cobolimab) in 2L NSCLC patients have progressed on prior therapy – P3 initiated Oct. 2022 – Significant market opportunity with 237,000 new NSCLC diagnoses per year in the US* • PERLA, H2H trial in 1L NSCLC: cORR of 46% for dostarlimab + chemo vs 37% in pembrolizumab + chemo Dostarlimab: 1L Ovarian Cancer • P3 FIRST trial (combination of dostarlimab + niraparib) in 1L ovarian cancer – P3 data (interim analysis) 2H 2023 – Significant market opportunity with ~20,000 new ovarian diagnoses per year in US* Additional Dostarlimab Royalty Opportunities • Dostarlimab combination with anti-TIGIT (EOS- 448/GSK’859A) in P2 for 1L NSCLC and H&NSCC • Dostarlimab + GDK4074386 in CITRINO trial across multiple solid tumors • Additional P1/2 dostarlimab combinations include: anti-CD96, STING agonist, and PVRIG across multiple solid tumors Immuno-Oncology Financial Collaboration JEMPERLI (dostarlimab) potential first-in-class PD-1 antagonist in first line endometrial and ovarian cancer *NCI SEER Data